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Kendall H. Lee, Frederick L. Hitti, Mark H. Shalinsky, Uhnoh Kim, James C. Leiter and David W. Roberts


The mechanism of action whereby high-frequency stimulation (HFS) in the thalamus ameliorates tremor and epilepsy is unknown. The authors studied the effects of HFS on thalamocortical relay neurons in a ferret in vitro slice preparation to test the hypothesis that HFS abolishes synchronized oscillations by neurotransmitter release.


Intracellular and extracellular electrophysiological recordings were made in thalamic slices. The neurons in the thalamic slice spontaneously generated spindle oscillations, and treatment with picrotoxin, a γ-aminobutyric acid A receptor antagonist, resulted in 3- to 4-Hz absence seizurelike activity. High-frequency stimulation (stimulation parameters: 10–1000-µA amplitude; 100-µsec pulse width; 100-Hz frequency; 1–60 seconds) was applied using a concentric bipolar stimulating electrode placed adjacent to the recording electrodes.

High-frequency stimulation within the thalamus generated inhibitory and excitatory postsynaptic potentials, membrane depolarization, an increase in action potential firing during the stimulation period, and abolished the spindle oscillations in the thalamocortical relay neurons. High-frequency stimulation applied to 20-µM picrotoxin-treated slices eliminated the 3- to 4-Hz absence seizurelike activity.


High-frequency stimulation eliminates spontaneous spindle oscillations and picrotoxin-induced absence seizurelike activity in thalamic slices by synaptic neurotransmitter release; thus, HFS may abolish synchronous oscillatory activities such as those that generate tremor and seizures. Paradoxically, HFS, which is excitatory, and surgical lesions of the ventrointermedius thalamus, which are presumably inhibitory, both suppress tremors. This paradox is resolved by recognizing that HFS-mediated neurotransmitter release and thalamic surgery both disrupt the circuit generating tremor or seizure, albeit by different mechanisms.

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J. Brett Fleming, Brian L. Hoh, Scott D. Simon, Babu G. Welch, Robert A. Mericle, Kyle M. Fargen, G. Lee Pride, Phillip D. Purdy, Chevis N. Shannon and Mark R. Harrigan


Postprocedural rebleeding is a significant source of morbidity following endovascular treatment of ruptured intracranial aneurysms. Previous large-scale reports include the Cerebral Aneurysm Rerupture After Treatment trial, the International Subarachnoid Aneurysm Trial, and the study on Early Rebleeding after Coiling of Ruptured Cerebral Aneurysms, which reported nonprocedural rebleeding rates within 30 days of treatment of 2.7%, 1.9%, and 1.4%, respectively. However, coiling of intracranial aneurysms is in a state of continual change due to advancing device design and evolving techniques. These studies included only patients initially treated prior to 2004. In the present study the authors assess the most recent short-term results with endovascular treatment of ruptured aneurysms.


A multicenter retrospective chart review was conducted of patients undergoing endovascular treatment for ruptured intracranial aneurysms between July 2004 and October 2009. The technique used, including the use of stent or balloon assistance, was evaluated. Demographic and clinical factors, such as sex, age, initial clinical presentation, aneurysm size, aneurysm location, and modified Raymond Classification following initial treatment, were also evaluated and compared between the groups in which rebleeding did and did not occur.


A total of 469 patients underwent endovascular treatment for a ruptured aneurysm; nonprocedural rehemorrhage occurred within 30 days of the initial coiling in 4 cases (0.9%). Two patients (50%) died after rehemorrhage. Stent-assisted coiling was used during the original treatment in 1 (25%) of the 4 patients with a rerupture. However, no technical, clinical, or demographic factors were found to be statistically significant in association with rebleeding.


Recent data suggest that the periprocedural rebleeding rate may be improving over time.

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Damian A. Almiron Bonnin, Matthew C. Havrda, Myung Chang Lee, Linton Evans, Cong Ran, David C. Qian, Lia X. Harrington, Pablo A. Valdes, Chao Cheng, Chris I. Amos, Brent T. Harris, Keith D. Paulsen, David W. Roberts and Mark A. Israel


5-aminolevulinic acid (5-ALA)–induced protoporphyrin IX (PpIX) fluorescence is an effective surgical adjunct for the intraoperative identification of tumor tissue during resection of high-grade gliomas. The use of 5-ALA-induced PpIX fluorescence in glioblastoma (GBM) has been shown to double the extent of gross-total resection and 6-month progression-free survival. The heterogeneity of 5-ALA-induced PpIX fluorescence observed during surgery presents a technical and diagnostic challenge when utilizing this tool intraoperatively. While some regions show bright fluorescence after 5-ALA administration, other regions do not, despite that both regions of the tumor may be histopathologically indistinguishable. The authors examined the biological basis of this heterogeneity using computational methods.


The authors collected both fluorescent and nonfluorescent GBM specimens from a total of 14 patients undergoing surgery and examined their gene expression profiles.


In this study, the authors found that the gene expression patterns characterizing fluorescent and nonfluorescent GBM surgical specimens were profoundly different and were associated with distinct cellular functions and different biological pathways. Nonfluorescent tumor tissue tended to resemble the neural subtype of GBM; meanwhile, fluorescent tumor tissue did not exhibit a prominent pattern corresponding to known subtypes of GBM. Consistent with this observation, neural GBM samples from The Cancer Genome Atlas database exhibited a significantly lower fluorescence score than nonneural GBM samples as determined by a fluorescence gene signature developed by the authors.


These results provide a greater understanding regarding the biological basis of differential fluorescence observed intraoperatively and can provide a basis to identify novel strategies to maximize the effectiveness of fluorescence agents.

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Oral Presentations

2010 AANS Annual Meeting Philadelphia, Pennsylvania May 1–5, 2010